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1.
Thromb Haemost ; 112(6): 1151-8, 2014 Dec.
Article in English | MEDLINE | ID: mdl-25208561

ABSTRACT

Flavanoid-rich dark chocolate consumption benefits cardiovascular health, but underlying mechanisms are elusive. We investigated the acute effect of dark chocolate on the reactivity of prothrombotic measures to psychosocial stress. Healthy men aged 20-50 years (mean ± SD: 35.7 ± 8.8) were assigned to a single serving of either 50 g of flavonoid-rich dark chocolate (n=31) or 50 g of optically identical flavonoid-free placebo chocolate (n=34). Two hours after chocolate consumption, both groups underwent an acute standardised psychosocial stress task combining public speaking and mental arithmetic. We determined plasma levels of four stress-responsive prothrombotic measures (i. e., fibrinogen, clotting factor VIII activity, von Willebrand Factor antigen, fibrin D-dimer) prior to chocolate consumption, immediately before and after stress, and at 10 minutes and 20 minutes after stress cessation. We also measured the flavonoid epicatechin, and the catecholamines epinephrine and norepinephrine in plasma. The dark chocolate group showed a significantly attenuated stress reactivity of the hypercoagulability marker D-dimer (F=3.87, p=0.017) relative to the placebo chocolate group. Moreover, the blunted D-dimer stress reactivity related to higher plasma levels of the flavonoid epicatechin assessed before stress (F=3.32, p = 0.031) but not to stress-induced changes in catecholamines (p's=0.35). There were no significant group differences in the other coagulation measures (p's≥0.87). Adjustments for covariates did not alter these findings. In conclusion, our findings indicate that a single consumption of flavonoid-rich dark chocolate blunted the acute prothrombotic response to psychosocial stress, thereby perhaps mitigating the risk of acute coronary syndromes triggered by emotional stress.


Subject(s)
Cacao , Candy , Functional Food , Stress, Psychological/therapy , Thrombosis/prevention & control , Acute Disease , Adult , Biomarkers/blood , Catechin/blood , Epinephrine/blood , Factor VIII/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinogen/metabolism , Healthy Volunteers , Humans , Male , Mathematical Concepts , Middle Aged , Norepinephrine/blood , Single-Blind Method , Speech , Stress, Psychological/blood , Stress, Psychological/diagnosis , Stress, Psychological/etiology , Switzerland , Thrombosis/blood , Thrombosis/diagnosis , Time Factors , Treatment Outcome , Young Adult , von Willebrand Factor/metabolism
2.
Heart ; 90(8): 853-8, 2004 Aug.
Article in English | MEDLINE | ID: mdl-15253951

ABSTRACT

OBJECTIVE: To investigate whether stimulated monocyte cytokine release and its inhibition by glucocorticoids differs between men and women. DESIGN: In vitro monocyte interleukin 6 (IL-6) and tumour necrosis factor alpha (TNFalpha) release after lipopolysaccharide stimulation were assessed with and without co-incubation with increasing doses of dexamethasone and hydrocortisone separately. Glucocorticoid sensitivity was defined as the amount of a particular glucocorticoid required to inhibit lipopolysaccharide stimulated monocyte cytokine release by 50%. The established cardiovascular risk factors of age, body mass index, number of cigarettes smoked daily, low density cholesterol to high density cholesterol ratio, systolic and diastolic blood pressure, and haemoglobin A1c were used as covariates. SETTING: Aircraft manufacturing plant in southern Germany. PATIENTS: 269 middle aged male and 36 middle aged female employees. RESULTS: Release of monocyte IL-6 and TNFalpha (each p = 0.001) was higher in samples from men than in those from women. Inhibition of lipopolysaccharide stimulated IL-6 and TNFalpha release by either glucocorticoid was less pronounced in samples from men than in those from women (IL-6: dexamethasone p = 0.033, hydrocortisone p = 0.029; TNFalpha: dexamethasone p < 0.001, hydrocortisone p = 0.089). CONCLUSIONS: The finding suggests that proinflammatory activity of circulating monocytes is higher in men than in women independent of cardiovascular risk factors, thereby providing one explanation for the relatively greater coronary risk in men.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Cardiovascular Diseases/etiology , Cytokines/metabolism , Dexamethasone/pharmacology , Hydrocortisone/pharmacology , Monocytes/metabolism , Adult , Cytokines/antagonists & inhibitors , Female , Humans , Interleukin-6/antagonists & inhibitors , Interleukin-6/metabolism , Lipopolysaccharides/pharmacology , Male , Monocytes/drug effects , Risk Factors , Sex Factors , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Necrosis Factor-alpha/metabolism
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